The intestinal microbiota is a diverse and dynamic ecosystem,1 which has developed a mutualistic relationship with its host and plays a crucial role in the development of the host's innate and adaptive immune responses.2 This ecosystem serves the host by protecting against pathogens, harvesting otherwise inaccessible nutrients, aiding in neutralisation of drugs and carcinogens, and affecting the metabolism of lipids.3 Gut bacteria modulate intestinal motility, barrier function and visceral perception.4
An interaction between the intestinal microbiota and the central nervous system (CNS) may seem difficult to conceive at first sight, but clinicians are well aware of the benefit of oral antibiotics and laxatives in the treatment of hepatic encephalopathy.5 Data accumulated from animal studies indicate that there is central sensing of gastrointestinal infections. For example, acute infection with Campylobacter jejuni results in anxiety-like behaviour and rapid activation of vagal pathways prior to onset of immune responses,6 while chronic Helicobacter pylori infection in mice leads to abnormal feeding behaviour and upregulation of tumour necrosis factor &#945; (TNF&#945;) in the median eminence of the hypothalamus.7 Rapid and sustained gut&#65533;brain communication may confer a significant advantage to the host, as central activation in response to changes in commensals or pathogens would allow better control of gut function and immunity.